Histone deacetylase 10 (HDAC10) belongs to the class IIb HDAC family and its biological role remains mostly unidentified. A decreased HDAC10 expression has been reported in patients with aggressive solid tumors (Osada et al. Int J Cancer 112: 26-32, 2004; Jin et al. Int J Clin Exp Pathol 7: 5872-5879, 2014), suggesting that loss of HDAC10 expression might confer a survival advantage to malignant cells. Consequently, results from our lab suggests that overexpression of HDAC10 in aggressive mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL) Z138c and MEC1 cells, respectively, resulted in a rapid induction of cell death in vitro with only 5 % of cells being alive at 48 h, cell cycle arrest, and up-regulation of co-stimulatory molecules. Here we present several standard methods to study the function of HDAC10 in B cell malignancies.
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http://dx.doi.org/10.1007/978-1-4939-3667-0_10 | DOI Listing |
Cell Signal
December 2024
Department of Rehabilitation, School of Medical Technology, Tianjin Medical University, Tianjin 300070, China. Electronic address:
This study aimed to investigate the underlying mechanisms by which physical exercise mitigates muscle atrophy induced by Dexamethasone (Dex). A muscle atrophy model was established in the mouse C2C12 cell line and 8-week-old mice treated with Dex, with subsequent verification of phenotype and atrogene expression. The potential benefits of combined aerobic and resistance exercise in mitigating muscle atrophy were then examined.
View Article and Find Full Text PDFBioorg Chem
December 2024
The State Key Laboratory of Chemical Oncogenomics, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, China; Institute of Biomedical Health Technology and Engineering, Shenzhen Bay Laboratory, Shenzhen, 518132, China; School of Pharmaceutical Sciences, Tsinghua University, Beijing, 100084, China.
The down-regulation of p21 after long-term CDK4/6 inhibition represents a key mechanism causing resistance to CDK4/6 inhibitors in some tumor cells, while the HDAC inhibitor could upregulate the level of p21. Herein, a series of novel CDK4/6 and HDAC dual-targeting inhibitors based on the moiety of palbociclib were designed and synthesized. Among them, compound N14 potently inhibited CDK4/6 and HDAC1/6 at nanomolar levels and induced cell apoptosis and G/G phase arrest through HDAC-p21-CDK signaling pathway in HuH-7 cell line.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
High glucose (HG) induced endothelial senescence is related to endothelial dysfunction and cardiovascular complications in diabetic patients. Humanin, a member of mitochondrial derived peptides (MDPs), is thought to contribute to aging-related cardiovascular protection. The goal of the study is to explore the pathogenesis of HG-induced endothelial senescence and potential anti-senescent effects of Humanin.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Pharmacy, The Second Affiliated Hospital of Dalian Medical University, #467 Zhongshan Road, Dalian, 116023, Liaoning, China.
Sodium-glucose co-transport protein 2 (SGLT2) inhibitors, a novel category of oral hypoglycemic agents, offer a promising outlook for individuals experiencing heart failure with reduced ejection fraction. Evidence is emerging that highlights their potential in alleviating myocardial fibrosis and oxidative stress. However, the precise mechanisms through which SGLT2 inhibitors influence myocardial fibrosis induced by angiotensin II (Ang II) or transforming growth factor-β1 (TGF-β1) are not fully understood.
View Article and Find Full Text PDFJ Gastroenterol Hepatol
December 2024
Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA.
Aim: The goal of this study was to determine the role of histone deacetylase 9 (HDAC9) in the development of diet-induced metabolic dysfunction-associated steatohepatitis (MASH) and white adipose tissue (WAT) dysfunctions.
Methods: We fed male and female mice with global Hdac9 knockout (KO) and their wild-type (WT) littermates an obesogenic high-fat/high-sucrose/high-cholesterol (35%/34%/2%, w/w) diet for 20 weeks.
Results: Hdac9 deletion markedly inhibited body weight gain and liver steatosis with lower liver weight and triglyceride content than WT in male mice but not females.
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